R. Ikegawa et al., POTENT INHIBITION OF THE PROINFLAMMATORY RESPONSES OF HUMAN POLYMORPHONUCLEAR CELLS BY PROSTAGLANDIN E-1 BUT NOT BY PGI(2) OR CARBACYCLIN, PROSTAGLANDINS & OTHER LIPID MEDIATORS, 55(2-3), 1998, pp. 95-107
The effects of prostaglandin E-1 (PGE(1)) on adhesion of activated hum
an polymorphonuclear cells (HPMNs) tg human umbilical vein endothelial
cells (HUVECs) and on chemotaxis of HPMNs were compared with those of
prostaglandin I-2 (PGI(2)) or its chemically stable analog carbacycli
n. Although HUVECs treated with PGI(2) inhibited only fMLP-activated H
PMN adhesion, both HUVECs and HPMNs treated with PGE(1) equally inhibi
ted HPMN adhesion, thus indicating the appropriate reactions to endoth
elium-leukocyte interaction by PGE(1). In the presence of a nonspecifi
c phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), PGE(
1) inhibited HPMN chemotaxis induced by either fMLP or LTB4 whereas bo
th PGI(2) and carbacyclin had no effect. To examine whether the respon
se of PMNs to PGs is species-specific, intracellular cAMP accumulation
in response to PGs was determined in human, guinea-pig, and rat isola
ted PMNs. Although PGE(1) increased cAMP levels in all PMNs tested, bo
th PGI(2) ana carabacyclin increased cAMP only in rat PMNs; These resu
lts demonstrate that HPMN cAMP formation can be affected by PGE(1) but
not by PGI(2). The findings help our understanding of the clinical us
e of PGs in patients with peripheral arterial occlusive diseases.